Public Release: 

New treatment approach to limit damage after joint bleed

Targeting Interleukin-1β may protect cartilage after trauma, major joint surgery or from bleeding due to hemophilia

European League Against Rheumatism

Rome, Italy, 12 June 2015: The results of a study presented today at the European League Against Rheumatism Annual Congress (EULAR 2015) identified that the cytokine (cell signalling protein) Interleukin-1β (IL-1β) is a crucial factor in the development of blood-induced cartilage damage. This finding opens up the possibility that a treatment targeting IL-1β could provide a new way to protect cartilage after a joint bleed, which in turn should significantly reduce subsequent disability.1

Exposure of joint cartilage to blood can occur after joint trauma, major joint surgery, or due to haemophilia. Joint bleeds, from whatever cause, are expected to lead to an inflammatory response in the joint and to significant destruction of joint cartilage. , Any treatment that could limit the damage resulting from a joint bleed would potentially make a big difference to minimising future disability.

"As therapeutic agents opposing the activity of IL-1β are readily available, further research is now warranted to investigate whether an IL-1β antagonist would be effective in preventing and treating joint damage as a result of bleeding into the joint," said Dr. Simon Mastbergen, principle investigator from the University Medical Centre Utrecht, Netherlands. "Findings also suggest that the quicker treatment is initiated, the less damage to the joint may be sustained," he added.

In contrast, blocking another cytokine - tumour necrosis factor-alpha (TNF-α) - exhibited no effect on blood-induced cartilage damage. "This would appear to rule out TNF-α inhibitors, a class of drug currently used to treat various forms of arthritis, for this new indication," Dr. Mastbergen concluded.

Healthy human cartilage samples were cultured for 4 days in the presence or absence of 50% whole blood. Either IL-1β monoclonal antibody, IL-1 receptor antagonist, or TNF-α monoclonal antibody was added during blood exposure. Subsequent cartilage damage was assessed.

Addition of IL-1β monoclonal antibody or IL-1 receptor antagonist resulted in a dose- and time-dependent protection of cartilage from blood-induced damage, with early administration after blood-exposure found to be the most beneficial. In higher concentrations, almost complete normalisation of cartilage was achieved. In contrast, addition of TNF-α monoclonal antibody exhibited no effect on blood-induced cartilage damage.

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Abstract Number: OP0262

NOTES TO EDITORS:
For further information on this study, or to request an interview with the study lead, please do not hesitate to contact the EULAR congress Press Office in Room 5B of Fiera Roma during EULAR 2015 or on:
Email: eularpressoffice@cohnwolfe.com
Onsite tel: +44 (0) 7738 890 799 / +44 (0) 20 7331 5442
Twitter: @EULAR_Press
Youtube: Eular Pressoffice

About EULAR

The European League Against Rheumatism (EULAR) is an umbrella organisation which represents scientific societies, health professional associations and organisations for people with rheumatic diseases throughout Europe.

EULAR aims to promote, stimulate and support the research, prevention, and treatment of rheumatic diseases and the rehabilitation of those it affects.

With 45 scientific member societies, 35 People with Arthritis and Rheumatism in Europe (PARE) organisations, 19 health professionals associations and 21 corporate members, EULAR highlights the importance of combating rheumatic diseases through both medical means and patient care.

EULAR 2015 is set to be the biggest rheumatology event in Europe with around 14,000 scientists, physicians, allied health professionals and related audiences in attendance from more than 120 countries. Over the course of the congress there will be some 300 oral and just under 2,000 poster abstract presentations, more than 150 sessions, 400 lectures, 40 poster tours and 350 invited speakers.

To find out more about the activities of EULAR, visit: http://www.eular.org

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